Studies of early hepatocellular proliferation and peroxisomal proliferation in Wistar rats treated with herbicide diclofop.

A study was performed to determine whether diclofop (2-(4-(2,4-dichlorophenoxy) phenoxy)propionic acid), introduced as a herbicide, exhibits the properties of peroxisome proliferators (PPs). Diclofop was administered orally at 7-56 mg/kg body weight per day to male Wistar rats for 2, 4, 7 or 14 consecutive days and some effects regarded as early hepatic markers of PPs were studied. The early changes in rat liver, produced by short-term treatment with diclofop consisted of mitogenesis and, time- and dose-related increase in liver weight. Hepatomegaly was typically associated with proliferation of smooth endoplasmic reticulum (SER) and peroxisomes. The parallel biochemical measurements showed that there was a dose-dependent increase in peroxisomal palmitoyl-CoA oxidation and catalase activity in treated rats. Markers of hepatocellular proliferation (S- and M-phase) indicated that mitogenesis was transient and declined despite continuation of diclofop treatment. The threshold exposure level for the palmitoyl-CoA oxidation (one of the peroxisome proliferation markers) was approximately the same (14 mg/kg body weightxper day) as for the stimulation of mitogenesis in Wistar rats. However, for hepatomegaly and catalase activity the threshold exposure level was 7 mg/kg body weightxper day. The results presented here demonstrate clearly that diclofop belongs to a class of rodent PPs.

Wilson's disease coexisting with viral hepatitis type C: a case report with histological and ultrastructural studies of the liver.

Histopathological and ultrastructural findings in the liver of a female patient who suffered from Wilson's disease (WD) and viral hepatitis type C (HCV) are reported. Light and electron microscopy examinations demonstrated a variety of morphological alterations--many of them frequently seen in livers of patients with WD and others that can be found in cases presenting HCV infection. The influence of coexistence of these two diseases on morphological changes is discussed.

Possible sexual transmission of Q fever among humans.

Direct transmission of Q fever between persons who have been exposed to Coxiella burnetii and their family members has been hypothesized on the basis of the results of serological surveillance. We studied nine shepherds who were employed in Spain during the sheep shearing season. After they returned to Poland, Q fever was detected in these shepherds and their wives. The titers of serum antibodies to phase I C. burnetii antigens ranged from 0 to 64 in patients with Q fever and in their spouses, and the titer of serum antibodies to phase II antigens ranged from 0 to 1.024 in patients and their spouses. Other family members were seronegative for antibodies to C. burnetii. C. burnetii strains were isolated from urine and semen samples obtained from patients with Q fever. Attached bacteria have been detected in spermatozoal cells observed with use of scanning electron microscopy.

NG-monomethyl-L-arginine increases platelet deposition on damaged endothelium in vivo. A scanning electron microscopic study.

There is increasing evidence that nitric oxide (NO) synthetized in vascular endothelium and in platelets by NO synthase influences vascular tone, down regulates platelet function and platelet-vessel wall interaction both in vitro and in vivo. We investigated the effect of a NO synthase inhibitor, NG-mono-methyl-L-arginine (L-NMMA, 100 mg/kg iv) on platelet-endothelial cell interaction in rabbit arteries ex vivo using scanning electron microscope (SEM). The effect of L-NMMA was examined on intact endothelium and on that damaged by arterial constriction. The infusion of L-NMMA increased systemic blood pressure and decreased carotid blood flow, however, it did not change the appearance of an intact endothelium and did not result in platelet activation on intact endothelial cells. In contrast, SEM of endothelial areas damaged by constriction showed extensive platelet adhesion and aggregation on subendothelium. These morphological changes were not detected in control animals with intact or damaged by arterial constriction endothelium. These results show that under physiological conditions, the inhibition of NO synthase alone does not result in platelet activation in vivo. However, when combined with endothelial injury it may lead to platelet activation and thrombosis.

The effect of organic chlorine compounds and their metabolites present in human milk on newborn mice.

The effect of pesticides and their metabolites (DDE, DDT, DDD, alpha, beta and gamma-HCH and PCBs) isolated from human milk on the blood and liver morphology of the mouse were studied. Mouse neonates were fed an extract of the organochlorine compounds in linseed oil for a period of 6 weeks. The lowest dose used in the experiment equalled that which a human infant can receive with its mother's milk, calculated per gram of body weight. Doses 10 and 100 times higher were also used. At the end of the experiment, tissue samples for electron microscopy and blood samples for haemotological examination were taken. Haematological examinations, in mice receiving pesticides, revealed a significant rise in the number of Heinz bodies in erythrocytes and an increased number of lymphocytes. These changes were related to the concentrations of the organic chlorine compounds that the animals were given. Electronmicroscopy demonstrated that organochlorine pesticides at doses equal to that might be received by infants caused proliferation of the smooth endoplasmic reticulum in hepatocytes without any clear damage to other subcellular structures. Doses 10 and 100 times higher resulted in more extensive proliferation of the smooth endoplasmic reticulum, reduction of the rough elements of the endoplasmic reticulum and damage to mitochondria. The latest changes were associated with an increased number of prominent Kupffer cells and the appearance of immigratory cells with traits characteristic of lymphocytes and monocytes.

Morphology of the prolactin producing cells in androgen-sterilized female rats.

The aim of the study was to follow morphology of the prolactin producing cells in growing female rats with evoked "early androgen syndrome". The experiment was carried out on 3, 6 and 12-week-old animals. At the age of 3 weeks no changes in morphology of the prolactin cells were observed as compared to that of control animals. In 6 and 12-week-old animals the significant differences between androgenized and control animals were found. The prolactin cells differed both from those characteristic for normal females and normal males. The main characteristic features were: significantly smaller number of cells than in normal females, their stronger fluorescence and presence of large and giant prolactin cells similar to the so called "pregnancy cells". Possible factors responsible for the described above changes are discussed.